Myocardial protection during cardiac surgery.
Myocardial protection during cardiac surgery.
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心脏手术期间的心肌保护。
DOI：
10.1146/annurev.me.33.020182.001055
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发表时间：
1982
影响因子：
10.5
通讯作者：
B. Reitz
中科院分区：
文献类型：
--
作者：
B. Reitz
近年来，在了解心脏手术期间心肌损伤的原因、引入尽量减少这种损伤的措施以及改善手术本身的条件方面取得了重要进展。冠状动脉手术是这一进步的主要推动力，因为冷心脏停搏提供的松弛且静止的心肌极大地促进了小血管解剖的实施。自 1970 年以来，冠状动脉疾病的手术已从每年数千例增加到 1980 年的超过 100,000 例 (1)。冠状动脉搭桥手术技术的改进以及目前与此类手术相关的极低风险在很大程度上归功于心肌保存的改善。在 1955 年开始的心脏直视手术的第一个十年中，术后低心输出量通常被认为是继发于患者术前状况的。然而，到 1970 年，三个观察结果被接受：(a) 手术期间心肌保护不足被认为是术后低心输出量和死亡的主要原因 (2)； (b) 心肌保护不足与肌病的晚期发展有关，即使在成功进行价值置换或修复先天性缺陷后也是如此 (3, 4)； (c) 一种罕见且极端的术中损伤“石心”，被认为是严重肥大心脏术中心肌保护不良所继发的 (5)。这些观察结果清楚地反映了当时使用的心肌保护需要大幅改进。
In recent years there have been important advances in understanding causes of myocardial injury during cardiac surgery, in the introduction of mea sures to minimize this injury, and in improving the conditions for perform ing the surgery itself. Coronary artery surgery has been a major stimulus for this advance, since the flaccid and still myocardium provided by cold cardioplegic arrest greatly facilitates the performance of small-vessel anas tomoses. Since 1970, surgery for coronary artery disease has grown from several thousand procedures per year to more than 100,000 operations in 1980 (1). The improvement in operative technique for coronary artery bypass and the very low risk now associated with such procedures is in large part due to improved myocardial preservation. During the first decade of open heart surgery, which began in 1955, postoperative low cardiac output was usually believed to be secondary to the preoperative condition of the patient. However, by 1970 three observa tions were accepted: (a) inadequate myocardial protection during surgery was implicated as a major cause of postoperative low cardiac output and death (2); (b) inadequate myocardial protection was associated with the late development of myopathy, even after successful value replacement or repair of congenital defects (3, 4); and (c) a rare and extreme form of intraopera tive damage, "stoneheart," was recognized to be secondary to poor intraop erative myocardial protection of severely hypertrophied hearts (5). These observations clearly reflected the need for substantial improvement in myo cardial protection in use at that time.